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• W4384661650 abstract "Abstract Androgen deprivation therapy is given to suppress prostate cancer growth; however, some cells continue to grow hormone-independently as castration-resistant prostate cancer (CRPC). Sulfated glycosaminoglycans promote ligand binding to receptors as co-receptors, but their role in CRPC remains unknown. Using the human prostate cancer cell line C4-2, which can proliferate in hormone-dependent and hormone-independent conditions, we found that epidermal growth factor (EGF)-activated EGFR–ERK1/2 signaling via 3- O -sulfated heparan sulfate (HS) produced by HS 3- O -sulfotransferase 1 (HS3ST1) is activated in C4-2 cells under hormone depletion. Knockdown of HS3ST1 in C4-2 cells suppressed hormone-independent growth, and inhibited both EGF binding to the cell surface and activation of EGFR–ERK1/2 signaling. Gefitinib, an EGFR inhibitor, significantly suppressed C4-2 cell proliferation and growth of a xenografted C4-2 tumor in castrated mouse. Collectively, our study has revealed a mechanism by which cancer cells switch to hormone-independent growth and identified the key regulator as 3- O -sulfated HS." @default.
• W4384661650 created "2023-07-20" @default.
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• W4384661650 date "2023-07-18" @default.
• W4384661650 modified "2023-09-25" @default.
• W4384661650 title "Switching mechanism from AR to EGFR signaling via 3-O-sulfated heparan sulfate in castration-resistant prostate cancer" @default.
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• W4384661650 doi "https://doi.org/10.1038/s41598-023-38746-x" @default.
• W4384661650 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37463954" @default.
• W4384661650 hasPublicationYear "2023" @default.
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